Transcript ACUTE COMPLICATIONS OF DIABETES MELLITUS

ACUTE COMPLICATIONS
OF DIABETES MELLITUS
Department of Internal Medicine №2
as.- prof. Martynyuk L.P.
• Diabetic ketoacidisis
Plan of
lecture
• Precipitating factors
• Signs, symptoms, physical examination, laboratory
findings
• Treatment
• Nonketonic hyperglycemichyperosmolar coma
• Precipitating factors
• Signs, symptoms, physical examination, laboratory
findings
• Treatment
• Lactoacidosis
• Precipitating factors
• Signs, symptoms, physical examination, laboratory
findings
• Treatment
• Hypoglycemic coma
• Precipitating factors
• Signs, symptoms, physical examination, laboratory
findings
• Treatment
Classification of acute
complications of DM
1. Diabetic coma:
1) ketosis→diabetic ketoacidisis (DKA)
2) nonketonic hyperglycemichyperosmolar coma (NKHHC)
3) lactoacidosis (LA)
2. Hypoglycemic coma (HC)
Precipitating factors of DKA
1.
newly diagnosed diabetes (presenting
manifestation);
2. inadequate administration of exogenous insulin;
3. increased requirements for insulin caused by the
presence of an underlying stressful condition:
• an intercurrent infection (pneumonia, cholecyctitis);
• a vascular disorder (myocardial infarction, stroke);
• an endocrine disorder(hyperthyroidism,
pheochromocytoma);
• trauma;
• pregnancy;
• surgery
Treatment
The goals of therapy include:
1. Reduction of hyperglycemia
2. Rehydratation
3. Correction of electrolyte imbalance
4. Correction of acid-base imbalance
5. Investigation of precipitating factors,
treatment of complications.
Nonketonic hyperglycemic-hyperosmolar
coma (NKHHC or HNC).
HNC is a syndrome characterized by impaired
consciousness, sometimes accompanied by
seizures, extreme dehydration, , and extreme
hyperglycemia that is not accompanied by
ketoacidosis.
Predisposing factors
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HNC seems to occur spontaneously in about 5 – 7 % of
patients.
Infection (e.g., pneumonia, urinary tract infection, gramnegative sepsis) is underlying frequent precipitating cause.
Use of certain drugs has been associated with this condition:
steroids increase glucogenesis and antagonize the action of
insulin;
potassium-wasting diuretics (hypokalemia decreases insulin
secretion), e.g., thiazides, furosemide;
other drugs, e.g., propranolol, azathioprine, diazoxide.
Other medical conditions such as cerebrovascular accident,
subdural hematoma, acute pancreatitis, and severe burns
have been associated with HNC.
Use of concentrated glucose solutions, such as used in
peripheral hyperalimentation or renal dialysis, has been
associated with HNC.
HNC can be induced by peritoneal or hemodialysis, tube
feeding.
Physical examination
1. Severe dehydration is invariably present.
2. Various neurologic deficits (such as coma, transient
hemiparesis, hyperreflexia, and generalized
areflexia) are commonly present. Altered states of
consciousness from lethargy to coma are observed.
3. Findings associated with coexisting medical
problems (e.g., renal disease, cardiovascular
disease) may be evident.
Laboratory findings
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Extreme hyperglycemia (blood glucose levels from 30 mmoll/l
and over are common.
A markedly elevated serum osmolality is present, usually in
excess of 350 mOsm/l. (Normal = 290 mOsm/l).
The initial plasma bicarbonate averaged.
Serum ketones are usually not detectable, and patients are
not acidic.
Serum sodium may be high (if severe degree of dehydration
is present), normal, or high (when the marked shift of water
from the intracellular to the extracellular space due to the
marked hyperglycemia is present).
Serum potassium levels may be high (secondary to the
effects of hyperosmolality as it draws potassium from the
cells), normal, or low (from marked urinary losses from the
osmotic diuresis). But potassium deficiency exists.
Treatment
This condition is a medical emergency and the patient
should be placed in an intensive care unit.
Many of the management techniques recommended
for a patient with DKA are applicable here as well.
The goals of therapy include:
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rehydration;
reduction of hyperglycemia;
electrolytes replacement;
investigation of precipitating factors, treatment of
complications.
Lactic acidosis (LA).
DM is one of the major causes of LA, a serious condition
characterized by excessive accumulation of lactic acid
and metabolic acidosis.
The hallmark of LA is the presence of tissue hypoxemia,
which leads to enhanced anaerobic glycolysis and to
increased lactic acid formation.
The normal blood lactic acid concentration is 1mmol/l,
and the pyruvic to lactic ratio is 10:1. An increase in
lactic acid without concomitant rise in pyruvate leads
to LA of clinical importance.
Predisposing factors
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Heart and pulmonary failure (which leads to hypoxia).
Usage of bigyanids.
Alcohol intoxication.
Ketoacidosis (it is important to have a very high index of
suspection with respect to presence of LA).
Physical examination
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Acrocyanosis is common.
Tachycardia frequently is present, blood pressure
is decreased.
Poor skin tugor and dry skin may be prominent.
Hypothermia is common in LA.
Hyperpnea or Kussmaul respiration are present
and related to degree of acidosis.
Findings associated with coexisting medical
problems (e.g., renal disease, cardiovascular
disease) may be evident.
Laboratory findings
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Blood glucose level is not high
Glucosurea is absent.
Blood lactic acid is high.
Treatment of LA
LA is treated by correcting the underlying cause.
Oxygentherapy
Metylen blue (50 – 100 ml of 1 % solution i/v droply)
In severe cases, bicarbonate therapy should be used
(intravenously-infused 2,5 % sodium bicarbonates 1
to 2 l/day).
LA can be treated with low dose insulin regimens with
5 % glucose solution infusion.
Symptomatic therapy:
- Hydrocortisone (250 mg i/v)
- Unitiol (5% solution 10 ml i/v (1- 2 ml/10 kg)
- α-lipoid acid (berlition, espa-lipon)
Comparison of DCA, HNC and LA.
Hypoglycemia
It is a syndrome characterized by symptoms of
sympathetic nervous system stimulation or central
nervous system dysfunction that are provoked by an
abnormally low plasma glucose level.
Hypoglycemia represents insulin excess and it can
occur at any time.
Precipitating factors
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irregular ingestion of food;
extreme activity;
alcohol ingestion;
drug interaction;
liver or renal disease;
hypopituitarism and adrenal insufficiency.
Physical examination
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The skin is cold, moist.
Hyperreflexia can be elicited.
Hypoglycemic coma is commonly associated with
abnormally low body temperature
Patient may be unconsciousness.
Laboratory findings
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Low level of blood glucose
Treatment
Treatment
References.
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2.
3.
The Merck Manual of Diagnosis and Therapy
(seventeenth Edition)/ Robert Berkow, Andrew J.
Fletcher and others. – published by Merck Research
Laboratories, 1999. – P. 177 - 185.
Manual of Endocrinology and Metabolism (Second
Edition)/ Norman Lavin. – Little, Brown and Company.Boston-New York-Toronto-London, 1994. - P. 543560.
Endocrinology (A Logical Approach for Clinicians
(Second Edition)). William Jubiz.-New York: WC GrawHill Book, 1985. - P. 241 – 253.